This evidencealso confirms our speculation concerning the fact that the α-helixis “a protective” conformation adopted by the NPM1 C-terminaldomain to avoid the aggregation50 of thewild-type protein that instead occurs in AML mutated versions of thisprotein.79−82 Indeed, recently, we performed an analogue study employing Ru-basedcomplexes quite similar to the Os compound analyzed in the presentinvestigation:28 data indicated similarThT signal reductions and the formation of a coordination adduct betweenNPM1 264–277 and the metal complex with the releaseof the same ligands. The gene discussed is NPM1; the disease is acute myeloid leukemia.